BIOMAT Database Logo BIOMAT Database Logo

Resistance mechanisms to cancer chemotherapy. 2008

Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Drug Resistance Laboratory, Centre for Cancer Research and Cell Biology, Queen's University Belfast, Belfast, UK.

Resistance to chemotherapy ('drug resistance') is a fundamental problem that limits the effectiveness of many chemotherapies currently used to treat cancer. Drug resistance can occur due to a variety of mechanisms, such as increased drug inactivation, drug efflux from cancer cells, enhanced repair of chemotherapy-induced damage, activation of pro-survival pathways and inactivation of cell death pathways. In this article, we review some of the major mechanisms of drug resistance and discuss how new molecularly-targeted therapies are being increasingly used to overcome these resistance mechanisms.

UI MeSH Term Description Entries
D009369 Neoplasms New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms. Benign Neoplasm,Cancer,Malignant Neoplasm,Tumor,Tumors,Benign Neoplasms,Malignancy,Malignant Neoplasms,Neoplasia,Neoplasm,Neoplasms, Benign,Cancers,Malignancies,Neoplasias,Neoplasm, Benign,Neoplasm, Malignant,Neoplasms, Malignant
D004249 DNA Damage Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS. DNA Injury,DNA Lesion,DNA Lesions,Genotoxic Stress,Stress, Genotoxic,Injury, DNA,DNA Injuries
D004260 DNA Repair The removal of DNA LESIONS and/or restoration of intact DNA strands without BASE PAIR MISMATCHES, intrastrand or interstrand crosslinks, or discontinuities in the DNA sugar-phosphate backbones. DNA Damage Response
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000970 Antineoplastic Agents Substances that inhibit or prevent the proliferation of NEOPLASMS. Anticancer Agent,Antineoplastic,Antineoplastic Agent,Antineoplastic Drug,Antitumor Agent,Antitumor Drug,Cancer Chemotherapy Agent,Cancer Chemotherapy Drug,Anticancer Agents,Antineoplastic Drugs,Antineoplastics,Antitumor Agents,Antitumor Drugs,Cancer Chemotherapy Agents,Cancer Chemotherapy Drugs,Chemotherapeutic Anticancer Agents,Chemotherapeutic Anticancer Drug,Agent, Anticancer,Agent, Antineoplastic,Agent, Antitumor,Agent, Cancer Chemotherapy,Agents, Anticancer,Agents, Antineoplastic,Agents, Antitumor,Agents, Cancer Chemotherapy,Agents, Chemotherapeutic Anticancer,Chemotherapy Agent, Cancer,Chemotherapy Agents, Cancer,Chemotherapy Drug, Cancer,Chemotherapy Drugs, Cancer,Drug, Antineoplastic,Drug, Antitumor,Drug, Cancer Chemotherapy,Drug, Chemotherapeutic Anticancer,Drugs, Antineoplastic,Drugs, Antitumor,Drugs, Cancer Chemotherapy
D016896 Treatment Outcome Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series. Rehabilitation Outcome,Treatment Effectiveness,Clinical Effectiveness,Clinical Efficacy,Patient-Relevant Outcome,Treatment Efficacy,Effectiveness, Clinical,Effectiveness, Treatment,Efficacy, Clinical,Efficacy, Treatment,Outcome, Patient-Relevant,Outcome, Rehabilitation,Outcome, Treatment,Outcomes, Patient-Relevant,Patient Relevant Outcome,Patient-Relevant Outcomes
D016923 Cell Death The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability. Death, Cell
D017209 Apoptosis A regulated cell death mechanism characterized by distinctive morphologic changes in the nucleus and cytoplasm, including the endonucleolytic cleavage of genomic DNA, at regularly spaced, internucleosomal sites, i.e., DNA FRAGMENTATION. It is genetically programmed and serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth. Apoptosis, Extrinsic Pathway,Apoptosis, Intrinsic Pathway,Caspase-Dependent Apoptosis,Classic Apoptosis,Classical Apoptosis,Programmed Cell Death,Programmed Cell Death, Type I,Apoptoses, Extrinsic Pathway,Apoptoses, Intrinsic Pathway,Apoptosis, Caspase-Dependent,Apoptosis, Classic,Apoptosis, Classical,Caspase Dependent Apoptosis,Cell Death, Programmed,Classic Apoptoses,Extrinsic Pathway Apoptoses,Extrinsic Pathway Apoptosis,Intrinsic Pathway Apoptoses,Intrinsic Pathway Apoptosis
D019008 Drug Resistance, Neoplasm Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures. Antibiotic Resistance, Neoplasm,Antineoplastic Drug Resistance,Drug Resistance, Antineoplastic,Antineoplastic Agent Resistance,Neoplasm Drug Resistance,Resistance, Antineoplastic Agent,Resistance, Antineoplastic Drug

Related Publications

Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
[Mechanisms of molecular resistance to cancer chemotherapy].
January 1989, Duodecim; laaketieteellinen aikakauskirja,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Cancer, DNA repair mechanisms, and resistance to chemotherapy.
October 2001, Journal of the National Cancer Institute,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Mechanisms of Resistance to Chemotherapy in Gastric Cancer.
January 2016, Anti-cancer agents in medicinal chemistry,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Cellular resistance mechanisms in cancer and the new approaches to overcome resistance mechanisms chemotherapy.
April 2023, Saudi medical journal,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Mechanisms of Resistance to Neoadjuvant Chemotherapy in Breast Cancer.
December 2017, The New England journal of medicine,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
[Mechanisms of resistance of cancer stem cells to chemotherapy].
December 2017, Bulletin du cancer,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Mechanisms of drug resistance in cancer chemotherapy.
January 2005, Medical principles and practice : international journal of the Kuwait University, Health Science Centre,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Mechanisms of chemotherapy resistance in ovarian cancer.
January 2022, Cancer drug resistance (Alhambra, Calif.),
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Mechanisms of Multidrug Resistance in Cancer Chemotherapy.
May 2020, International journal of molecular sciences,
Kelly Marie Redmond, and Timothy Richard Wilson, and Patrick Gerard Johnston, and Daniel Broderick Longley
Chemotherapy Resistance Mechanisms in Advanced Skin Cancer.
March 2017, Oncology reviews,
Copied contents to your clipboard!